Objective:To explore the relationship between pulmonary function and coronary artery disease (CAD) with the severity of coronary artery lesions in relevant patients.
Methods:A total of 200 patients received coronary angiography (CAG) in our hospital were studied. The patients were divided into 2 groups: Non-CAD group, n=88 and CAD group, n=112. The degree of coronary stenosis was assessed by GENSINI score;the pulmonary function, echocardiography and fasting blood level of brain natriuretic peptide(BNP) were examined in all patients.
Results:Forced expiratory volume in 1 second (FEV1) in CAD group (2.33±0.54) L/1s was lower than Non-CAD group (2.63±0.39) L/1s, P=0.04. Multivariate logistic regression analysis indicated that decreased FEV1 was the independent risk factor for CAD (OR=2.9, 95%CI 1.89-4.23, P<0.01). Spearman correlation analysis showed that FEV1 was negatively related to blood level of BNP (r=-0.54, P<0.01), positively related to the ratio of E/A (r=0.27, P=0.03). GENSINI score was positively related to smoking (r=0.31, P=0.01), diabetes (r=0.19, P=0.03) and negatively related to FEV1 (r=-0.40, P<0.01). With adjusted variables, partial correlation analysis presented that FEV1 was negatively related to GENSINI score (r=-0.21, P=0.01).
Conclusion:Decreased FEV1 is not only related to CAD occurrence, but also related to the degree of coronary stenosis in relevant patients.

Objective To compare the effects of propofol and midazolam on the prognosis of patients treated with noninvasive positive pressure ventilation.Methods A prospective,single-blind,randomized controlled trial (RCT) was conducted in 90 patients who were treated with noninvasive ventilation for acute dyspnea in the ICU of the Sixth People's Hospital Affiliated to Shanghai Jiaotong University from October 2014 to December 2016.They were randomly divided into three groups according to the digital table,with 30 cases in each group.The control group was not given sedation treatment.The propofol group was given propofol 0.5 ～ 1 mg/kg,and then administered by intravenous infusion of 1 mg · kg-1 · h-1 with a micropump.The midazolam group was given midazolam 0.05-O.1 mg/kg,and then with intravenous infusion of 0.05-0.1 mg · kg-1 · h-1 maintaining the patients'sedation goals(Ramsay score of 2).The vital signs and blood gas analysis indicators were recorded.The incidence of tracheal intubation,the incidence of hospital infection,length of ICU and hospital stay,mortality and sedation-related complications were compared.Results The tracheal intubation rate in the propofol group was similar to that in the midazolam group (20.0％ vs.23.3％,x2 =2.65,P ＞ 0.05),while the tracheal intubation rate (46.7％) in the control group was significantly higher (x2 =4.21,4.17,all P ＜ 0.05).The length of ICU and hospital stay in the pmpofol group [(7 ± 3)d and (15 ± 5) d] and midazolam treatment group[(8 ± 4) d and (16 ± 4) d] were significantly shorter than those in the control group[(13 ± 4) d and (20 ± 6) d] (t =2.384,2.371,2.392,2.389,all P ＜ 0.05).The mortality rates of 30d (20.0％,6/30) and 90d (30.0％,9/30) in the control group were higher than those in the propofol group(10.0％,3/30;20.0％,6/30),and the midazolam group (13.3％,4/30;23.3％,7/30),but the differences were not statistically significant(P ＞ 0.05).The incidence rates of hospital infection in the pmpofol group and midazolam group were 6.6％ (2 cases) and 10.0％ (3 cases),which were significantly lower than 33.3％ (10 cases) in the control group (x2 =4.32,4.23,all P ＜ 0.05).Conclusion The use of mild sedation in patients of acute dyspnea treated with noninvasive positive pressure ventilation can improve the patients' tolerance rate,reduce the rate of tracheal intubation and the incidence of hospital infection,and decrease the length of ICU and hospital stay,without significant adverse reactions.There was no significant difference between propofol and midazolam.

Objective To investigate the protective mechanisms of Atorvastatin against high glucose environment-induced injuries of myocardial microvascular endothelial cells. Methods Myocardial microvascular endothelial cells(MMECs)in SD rat were cultured and divided into groups of control group ,hyperglycemia group ,atorvastatin group ,and atorvastatin + high glucose group. The level of reactive oxygen species (ROS)was assayed using Superoxide Assay Kit. Apoptosis of cells was detected by terminal deoxynucleotidyl transferase(TdT)-mediated dUTP nick end labeling(TUNEL) . The expression levels of Akt1 and β1-Integrin were assayed by short-interfering RNA (siRNA ) technique ,and the levels of small GTP-binding protein dissociation stimulator (SmgGDS) expression were measured using Western blot. Results (1)The level of ROS was higher in the high glucose group than in the control group(t=4.154 ,P <0.01) ,and lower in both Atorvastatin group and the Atorvastatin + high glucose group than in the high glucose group (t= 4.233 and 2.893 ,both P <0.05). (2)The proportion of apoptotic cells was higher in the high glucose group than in the control group(t= 4.058 ,P < 0.01) ,and lower in both Atorvastatin group and the Atorvastatin + high glucose group than in the high glucose group(t=4.157 and 2.601 ,both P<0.05).(3)The expression level of Akt1 was lower in the high glucose group and the high glucose + Atorvastatin group than in the mock control group after transfection of Akt1-siRNA(t=4.058 and 4.167 ,both P<0.01).The expression level of β1-integrin was lower in the high glucose group and the high glucose + atorvastatin group than in the mock control group after transfection of β1-integrin-siRNA (t=4.073 and 4.215 , both P<0.01). (4)Western blot analysis showed the following results. First ,the relative expression levels of SmgGDS in both the low dose(1 μmol/L)and high dose(10 μmol/L)of atorvastatin group were higher than in the control group (t= 2.671 and 2.832 ,both P < 0.05).Second ,the relative expression level of SmgGDS in the high dose group were higher than in the low dose group (t=2.612 , P< 0.05 ). Third ,after transfection of Akt1-siRNA ,the expression level of SmgGDS in the high glucose + Atorvastatin group and the high glucose group was decreased ;and the level was higher in the high glucose + atorvastatin + mock group than in the high glucose + mock group(t=4.051 ,P<0.01).Fourth ,after transfection of β1-integrin-siRNA ,the expression level of SmgGDS was lower in high glucose + Atorvastatin group and the high glucose group than in the high glucose +Atorvastatin + mock group ;the level was higher in the high glucose + Atorvastatin + mock group than in the high glucose + mock group(t= 4.068 ,P < 0.01).Fifth ,the expression level of Akt phosphorylation in the high glucose group and the high glucose + Atorvastatin group was higher at 10 minutes than at five minutes(t=2.608 ,P<0.05) ,and higher at 15 minutes than at 10 minutes(t=3.127 ,P <0.05). After transfection of β1-integrin-siRNA ,the expression level of p-Akt /t-Akt was lower in the high glucose group than in the high glucose + mock group(t= 3.371 ,P < 0.05). Conclusions Atorvastatin treatment protects myocardial microvascular endothelial cells possibly by up-regulating SmgGDS through β1-integrin/Akt1 against high glucose environment-induced oxidative stress and apoptosis injuries.